Case Studies in Toxicology: An Unlikely Cause of Paralysis
What is hypokalemic periodic paralysis?
Hypokalemic periodic paralysis (HypoKPP) is a syndrome of episodic muscle weakness with concomitant hypokalemia. Familial forms of HypoKPP have been attributed to mutations in genes coding for either calcium or sodium channels.
The nonfamilial form of HypoKPP is attributed to hyperthyroidism and is most often seen in Asian men in the second and third decades of life. The disorder is characterized by acute onset hypokalemia and extremity paralysis with simultaneous hyperthyroid state. It is believed that hypokalemia occurs as a result of intracellular shift of potassium from thyroid-induced hormone sensitization of the Na+/K+-ATPase rather than a depletion of total body potassium. Acute episodes of paralysis are triggered by high-carbohydrate meals, alcohol consumption, emotional stress, and infection. Paralysis can last from 3 to 96 hours and is accompanied by decreased or absent deep tendon reflexes with normal sensation and mental status.
In the nonfamilial form of HypoKPP, signs of thyrotoxicosis are often present and include tachycardia, moist skin, and hyperthermia, but it may be difficult to specifically recognize this etiology given the patient’s grave clinical condition.4 Similar to many significant metabolic and electrolyte disturbances, complications of HypoKPP include dysrhythmia, respiratory failure, and sometimes death.5
How should HypoKPP be managed in the ED?
Management of HypoKPP begins with careful assessment of the patient’s airway, breathing, and circulation. Once the patient is stabilized, management of consequential effects of hypokalemia, such as respiratory distress and muscular paralysis, should focus on correcting the electrolyte and endocrine derangements.
Propranolol. If the patient exhibits signs of thyrotoxicosis, initial treatment includes propranolol, a nonselective beta-blocker, which both prevents the intracellular shift of potassium and assists in correcting the underlying hyperthyroid and hypermetabolic state. Although there is no standard propranolol dosing protocol for HypoKPP, some authors suggest that an aggressive dose of 2 mg intravenously (IV) every 10 minutes can shorten the patient’s episode of paralysis to 6 hours.6
Potassium Chloride. Administration of potassium chloride to raise the serum potassium to life-sustaining concentrations should be done cautiously through IV infusion of standard doses.7 In correcting hypokalemia with potassium, care should be taken to avoid overcorrection, which may subsequently result in rebound hyperkalemia as the total body potassium redistributes. Lower doses of potassium (ie, <50 mEq per dose), are preferred to achieve adequate repletion while avoiding rebound hyperkalemia.8
Case Conclusion
The results of thyroid studies that had been added on to the original set of laboratory studies revealed profound hyperthyroidism, with an essentially absent concentration of thyroid-stimulating hormone.
